Swynghedauw B, Besse S, Assayag P, Carré F, Chevalier B, Charlemagne D, Delcayre C, Hardouin S, Heymes C, Moalic J M
INSERM, Hôpital Lariboisière, Paris, France.
Am J Cardiol. 1995 Nov 2;76(13):2D-7D. doi: 10.1016/s0002-9149(99)80484-6.
During aging, experimental studies have revealed various cellular changes, principal among which is myocyte hypertrophy, which compensates for the loss of myocytes and is associated with fibrosis. The expression of alpha-myosin heavy chain is replaced by that of the isogene beta-myosin, which leads to decreased myosin adenosine triphosphatase (ATPase) activity. In consequence, contraction is slower and more energetically economical. The Ca(2+)-ATPase of the sarcoplasmic reticulum and Na+/Ca2+ exchange activity are decreased, which probably explains the reduced velocity of relaxation. Membrane receptors are also modified, since the density of both the total beta-adrenergic and muscarinic receptors is decreased. The senescent heart is able to hypertrophy in response to overload and to adapt to the new requirements. Similar alterations are observed both in the senescent heart and in the overloaded heart, in clinical as well as in experimental studies; however, differences do exist, especially in terms of fibrosis and arrhythmias.
在衰老过程中，实验研究揭示了各种细胞变化，其中主要的是心肌细胞肥大，它可补偿心肌细胞的损失并与纤维化相关。α-肌球蛋白重链的表达被同基因的β-肌球蛋白所取代，这导致肌球蛋白三磷酸腺苷酶（ATPase）活性降低。因此，收缩更缓慢且在能量利用上更经济。肌浆网的Ca(2+)-ATP酶和Na+/Ca2+交换活性降低，这可能解释了舒张速度的降低。膜受体也发生改变，因为总的β-肾上腺素能受体和毒蕈碱受体的密度均降低。衰老的心脏能够对负荷过重做出肥大反应并适应新的需求。在临床和实验研究中，衰老心脏和负荷过重心脏均观察到类似的改变；然而，差异确实存在，尤其是在纤维化和心律失常方面。
